48
colon. The other possible mode of action by RS consumption involves modifying
the expression path of oncogenes to abscond the growth phase of the cell cycle
thereby allowing for differentiation of tumour cells to produce normal matured cells
(Young et al. 1995). Adults with pre neoplastic lesions in their colon may therefore
benefit from dietary RS (Liu and Xu 2008). A study conducted by Bingham et al.
(2003) invariably showed the reductive effect of dietary fibre on the prevalence of
colorectal cancer on populations where in the average dose of dietary fibre was
doubled. Various studies examining the protective effect of resistant starch on
colonic cancer have been conducted on both animals generally focusing on mice
and rats as well as human subjects. In animal models tumours induced by mutagens
like dimethyl hydrazine or azoxy methane or by using genetic models of intestinal
tumours, a diet containing approximately 5.6% high amylose RS3 has been shown
to be effective in controlling the cluster formation of abnormal mass of glands in the
internal surface of colon and rectum of the animals (Perrin et al. 2001). Biopsy studies conducted on the subjects showed strong effect of butyrate on the development
and proliferation of the abnormal cell mass in the intestinal areas possibly because
of the inherent ability of resistant starch to lessen the bile acid concentration
(Grubben et al. 2001). Various other possible mechanisms involve the acidification
of the digestible material limiting the escalation of pathogenic microorganisms as
well as restraining the absorption and assimilation of toxic components like ammonia. This valuable effect of SCFA restricts the colonocyte contact with the mutagenic agents (Topping 2007). The effective role of SCFA in modifying various
physiological mechanisms including enhanced colonic muscle activity and muscle
oxygenation plus the improved colonic mucosal activity reducing the possible risks
of cell aberrations and lesions. The effect of RS was shown to be predominant on
the sites wherein the maximum fermentation of the starch took place (Young and Le
Leu 2004) but the protective effect was found to be ineffective towards the later
stages of colonic cancer development. Different studies have shown contradictory
results regarding the effect of resistant starch or its adjuncts on the colonic function.
In two separate experiments carried by Thorup et al. (1995) as well as Cassand et al.
(1997), RS was found to exert a protective effect against the development of aberrant tumours. However the reports published by negated any of these protective
effects. Similarly, Sakamoto and co-researchers (1996) found a meagre effect on
tumour development after the subjects were fed diets containing 10% RS. However
various studies extensively support the repressing activity of butyrate on the abnormal cell proliferation at physiological concentrations and increase in colorectal cancer cells apoptosis of CRC cells (Hague et al. 1993). Some studies have also reported
that the rapid tumor growth depends on glucose availability. The consumption of RS
has been associated with the reduction of the energy capacity of cells in preneoplastic lesions. As a result, RS enhances resistance to colonization, inhibits bacterial
translocation, and finally boosts the chemical and enzymatic functions, involved in
the protection of gastrointestinal tract (Roberfroid 2005). The increased motility of
the large intestine reduces the time that stool remains in the colon and relieves constipation symptoms. Increased stool transit time and constipation are among the risk
factors for colorectal cancer because fecal contact with the colon and rectal walls
G. Akhtar et al.
colon. The other possible mode of action by RS consumption involves modifying
the expression path of oncogenes to abscond the growth phase of the cell cycle
thereby allowing for differentiation of tumour cells to produce normal matured cells
(Young et al. 1995). Adults with pre neoplastic lesions in their colon may therefore
benefit from dietary RS (Liu and Xu 2008). A study conducted by Bingham et al.
(2003) invariably showed the reductive effect of dietary fibre on the prevalence of
colorectal cancer on populations where in the average dose of dietary fibre was
doubled. Various studies examining the protective effect of resistant starch on
colonic cancer have been conducted on both animals generally focusing on mice
and rats as well as human subjects. In animal models tumours induced by mutagens
like dimethyl hydrazine or azoxy methane or by using genetic models of intestinal
tumours, a diet containing approximately 5.6% high amylose RS3 has been shown
to be effective in controlling the cluster formation of abnormal mass of glands in the
internal surface of colon and rectum of the animals (Perrin et al. 2001). Biopsy studies conducted on the subjects showed strong effect of butyrate on the development
and proliferation of the abnormal cell mass in the intestinal areas possibly because
of the inherent ability of resistant starch to lessen the bile acid concentration
(Grubben et al. 2001). Various other possible mechanisms involve the acidification
of the digestible material limiting the escalation of pathogenic microorganisms as
well as restraining the absorption and assimilation of toxic components like ammonia. This valuable effect of SCFA restricts the colonocyte contact with the mutagenic agents (Topping 2007). The effective role of SCFA in modifying various
physiological mechanisms including enhanced colonic muscle activity and muscle
oxygenation plus the improved colonic mucosal activity reducing the possible risks
of cell aberrations and lesions. The effect of RS was shown to be predominant on
the sites wherein the maximum fermentation of the starch took place (Young and Le
Leu 2004) but the protective effect was found to be ineffective towards the later
stages of colonic cancer development. Different studies have shown contradictory
results regarding the effect of resistant starch or its adjuncts on the colonic function.
In two separate experiments carried by Thorup et al. (1995) as well as Cassand et al.
(1997), RS was found to exert a protective effect against the development of aberrant tumours. However the reports published by negated any of these protective
effects. Similarly, Sakamoto and co-researchers (1996) found a meagre effect on
tumour development after the subjects were fed diets containing 10% RS. However
various studies extensively support the repressing activity of butyrate on the abnormal cell proliferation at physiological concentrations and increase in colorectal cancer cells apoptosis of CRC cells (Hague et al. 1993). Some studies have also reported
that the rapid tumor growth depends on glucose availability. The consumption of RS
has been associated with the reduction of the energy capacity of cells in preneoplastic lesions. As a result, RS enhances resistance to colonization, inhibits bacterial
translocation, and finally boosts the chemical and enzymatic functions, involved in
the protection of gastrointestinal tract (Roberfroid 2005). The increased motility of
the large intestine reduces the time that stool remains in the colon and relieves constipation symptoms. Increased stool transit time and constipation are among the risk
factors for colorectal cancer because fecal contact with the colon and rectal walls
G. Akhtar et al.